Suchandan Sikder, Natasha L Williams, Alanna E Sorenson, Md A Alim, Miranda E Vidgen, Nicole J Moreland, Catherine M Rush, Robert S Simpson, Brenda L Govan, Robert E Norton, Madeleine W Cunningham, David J McMillan, Kadaba S Sriprakash, Natkunam Ketheesan
Acute rheumatic fever and rheumatic heart disease (ARF/RHD) have long been described as autoimmune sequelae of Streptococcus pyogenes or group A streptococcal (GAS) infection. Both antibody and T-cell responses against immunodominant GAS virulence factors, including M protein, cross-react with host tissue proteins, triggering an inflammatory response leading to permanent heart damage. However, in some ARF/RHD-endemic regions, throat carriage of GAS is low. Because Streptococcus dysgalactiae subspecies equisimilis organisms, also known as β-hemolytic group C streptococci and group G streptococci (GGS), also express M protein, we postulated that streptococci other than GAS may have the potential to initiate or exacerbate ARF/RHD...
June 20, 2018: Journal of Infectious Diseases